Neuro Exam 3

Somatosensation

how do we sense things in our bodies?

Pacinian corpuscle

• large vague borders

• fast adapting

• vibration

Meissner’s corpuscle

• small, sharp borders

• fast- adapting

• touch

Merkel’s discs

• small, sharp borders

• slow-adapting

• touch

Ruffini’s ending

• Large, vague borders

• slow adapting

• stretch

receptive fields

area on the body where a given neuron will respond to a stimulus

cerebrum (forebrain)

conscious control of movement

brain stem

direct movements

spinal cord

direct movements

subcortical basal ganglia

helps to produce the appropriate amount of force for movement

cerebellum

helps to regulate the timing and accuracy of movement

• involved in balance, fine motor control, posture/muscle tone

motor command direction

sent via efferent pathways which leave the spinal cord through the ventral roots

prefrontal cortex

plans complex behavior (volition)

premotor cortex

maps out the appropriate complex movement sequences (what is necessary to do a task)

• includes the coordination of multiple body parts

primary motor cortex

specifies and communicates how each movement is to be carried out

each area corresponds to the muscles of specific body parts

nociceptors

receptors expressed on free nerve endings

• respond to painful stimuli

• Adelta and c fivers carry this information to the CNS

A delta

Noxious and mechanical stimulus

C fiber

noxious heat and chemical stimuli

lateral corticospinal (dorsolateral)

controls contralateral distal limbs (descending)

anterior corticospinal (ventromedial)

controls trunk muscles and proximal limbs (descending)

spinal cord to muscle

neuromuscular joint

• in the space between nerves and muscle, Acetylcholine is used

basal ganglia

• projects back to motor cortex and substantia nigra

• helps to fine-tune voluntary movements

• inputs relay mapped sequence plan which is adjusted and relayed back to cortex

Basal ganglia input

• from multiple areas of cortex

• nigrostriatal dopaminergic system from the substantia nigra

hyperkinetic symptom

when damage to the caudate putamen causes unwanted writing and twitching (dyskinesias)

• Huntington’s and Tourette’s

Hypokinetic symptom

when damage to basal ganglia results in loss of motor ability, leading to rigidity and difficulty initiating and producing movement

• parkinson’s

Implicit memory

• unconscious

• retained skill, continued response, but can’t explicitly retrieve knowledge

explicit memory

• conscious

• can retrieve an item and are aware that they remembered the correct item

short-term

• involves frontal lobes

• briefly held in memory briefly then discarded

long-term memory

• involves temporal lobe

• info is held in memory for a lifetime

Patient HM

• had severe epileptic seizures from 10 yrs old

• his temporal lobe was removed including the hippocampus and amygdala (1953)

explicit anterograde memory

the inability to form new memories (usually starting from a traumaic event)

semantic

a type of explicit memory that recalls facts and information

episodic

a type of explicit memory that recalls events of life

explicit retrograde memory

remembering memories from the past (before traumatic event)

• recalling relatives

• daily tasks

• facts from school

explicit retrograde amnesia

temporarily graded (the further in the past = more likely to remember)

implicit memory test

drawing inside the lines of a star by only using a mirror to see

working memory

short term memory with limited capacity while manipulating those pieces of information

HM and explicit memory

he could not create new declarative memories

what did HM have intact?

• implicit memory

• working memory

• retrograde amnesia

what did HM not have intact?

• long term explicit memory formation

• explicit memory

Morris water maze

• measures spatial ability, memory, navigational skills

• hippocampal injury results in impairment finding the platform

radial arm maze

• 8 arms extend from center platform

• one end is baited with food and the # of entries is recorded

Long-term potentiation (LTP)

• long lasting enhancement of synaptic strength (cellular/molecular)

• basis for learning and memory (behavioral/clinical)

No stimulation

low stimulation

high stimulation

LTP

the cellular foundation of learning and memory

LTP at glutamatergic hippocampal synapse

it stimulates hippocampal inputs and records hippocampus neurons

• the high frequency stimulation causes enhanced glutamate release

LTP presynaptic modifications

Glutamate release (frequency/amount)

LTP at glutamatergic synapses (postsynaptic modifications)

At resting potential:

1) glutamate release

2) AMPA receptor activation

3) postsynaptic depolarization

During postsynaptic depolarization:

4) relief of Mg2+ block at NMDA receptor => more depolarization and Ca²+ entry

5) CaMKII activation => gene transcription, AMPAR phosphorylation, actin-induced structural changes, etc.

Spoon and apple test

apple is put in the right visual field, so the left parts of your eyes receive that information

• people with an intact corpus callosum first get this information in the left then passed to the right

• those without it can say apple but the left hand cannot grab it when asked to

Spoon is on the left visual field → right brain sees spoon

• without: cannot speak “spoon”, but left hand can reach under hood to select the spoon (right hand could not)

Commissurotomy

only the left hemisphere receives that information

holding object with left hand

1) put spoon into left hand

2) right brain feels spoon

• subject cannot say the word spoon, but were aware something was there

• left hand could choose another spoon

Anesthesia reversibly shuts down language

• sodium amytal test prior to surgery

• test is repeated for the other hemisphere

Dichotic listening task

left side of headphones says “ga” and participant repeats the syllable

imaging studies

• fMRI or PET

• more color => activity in those areas

chimeric faces test

determines which hemisphere is dominant for facial processing

the higher your laterality quotient, the more the left face is dominant (right hemisphere of brain)

Right hemisphere functions (better at)

music, spatial problem solving, facial processing

non-fluent aphasia (Broca’s)

has: normal comprehension of speech and written word

difficulty: producing speech, slow, inarticulate, omits pronouns, prepositions, conjunctions, tenses

writing: looks like a child’s

fluent aphasia (Wernicke’s)

• can: speak articulately but it is a “word salad”

• impaired comprehension and difficulty recalling names of objects

• Writing: looks more articulated but the sentences make no sense

rehabilitation with aphasia

• speech language training, TMS, medication

• demonstration of plasticity/learning

Schizophrenia (SZ)

• Affects 1% of people, more common in med

• diagnosed in 20s-30s

• risk factors in genetics and environment (ex. maternal stress)

positive symptoms (SZ)

delusions, hallucinations, disorganizations with speech, catatonia (motot abnormalities)

negative symptoms (SZ)

flat affective response, anhedonia (loss of pleasure)

Delusions

• altered persisting complex perception of themselves

• can occur after injury, schizophrenia, psychotic event

• can go away spontaneously

Capgras delusion (CS)

• perception that other people/objects have been replaced by an imposter

• “delusional misidentification syndrome”

• correlations between CS and Prosopagnosia (inability to recognize faces)

• patients have the conscious ability to recognize faces, but disruption to the system that facilitates emotional arousal to familiar faces

Possible reasoning for Capgras delusion

disconnection between the temporal cortex(fusiform face area), and the limbic system involved in emotions (amygdala)

Alzheimer’s disease (AD)

• Progressive neurodegenerative disease:

  • memory deficits. loss of speech, motor impairment

• cellular atrophy

• visual cortex is preserved

• entorhinal cortex, associative cortices (sensory, and allocortex (hippocampus) are in loss

findings in AD

• high levels of amyloid-beta plaques

• have tau tangles and hyperphosphorylation

  • tau is normally just on axons, for this disease is it in the whole cell

No fear conditioning

What does no amygdala mean for rats?

Fear response

rapid physiological changes in response to a perceived threat/danger

• increased heart rate, rapid breathing, dilated pupils, sweating

Amygdala

• located in basal ganglia/forebrain

• modulated hypothalamus: sympathetic/parasympathetic NS

• Emotional responding, especially fear

patient DR

• intractable seizures for years

• targeted lesions of amygdala in 1980s

• had difficulty recognizing some emotions in others (fear/anger)

fear conditioning in nonhumans

1) subject is exposed to a conditioned stimulus (light, tone)

2) foot shock results in freezing of movement

3) CS produced the conditioned response (freezing)

empathy in rats

rat will help trapped cage mate more often than a stranger

prairie vole

• experimental model for romantic love

• socially monogamous after mating

• also show social monogamy

• male spends more time with female partner and less with strangers (and vice versa)

• display increased anxiety after being separated from their partner

Chemical signals of romantic love

Vasopressin and oxytocin

• both produced by the hypothalamus and released by pituitary gland

oxytocin & vasopressin (voles)

• giving this increases pair bonding without mating

• blocking it decreases pair bonding after mating